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Książki na temat „Paget's disease of bone”

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Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 14 marca 2023

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1

Arthritis & Rheumatism Council for Research., red. Paget's disease of bone: An information booklet. Chesterfield: Arthritis & Rheumatism Council for Research, 1997.

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2

Kanis, John A. Pathophysiology and treatment of Paget's disease of bone. London: Martin Dunitz, 1991.

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3

National Institutes of Health (U.S.). Osteoporosis and Related Bone Diseases National Resource Center. Questions and answers about Paget's disease of bone. Bethesda, MD: NIH Osteoporosis and Related Bone Diseases National Resource Center, 2011.

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4

Singer, Frederick R., i Stanley Wallach, red. Paget’s Disease of Bone. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-2307-5.

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5

Symposium on the Treatment of Paget's Disease of Bone (1989 New York, N.Y.). Paget's disease of bone: Clinical assessment, present and future therapy : proceedings of the Symposium on the Treatment of Paget's Disease of Bone, held October 20, 1989 in New York City. New York: Elsevier, 1991.

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6

Khetarpal, Umang. In search of pathologic correlates for hearing loss and vertigo in Paget's disease: A clinical and histopathologic study of 26 temporal bones. St. Louis: Annals Pub. Co., 1990.

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7

R, Reid I., red. Metabolic bone disease. London: Baillière Tindall, 1997.

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8

Lecka-Czernik, Beata, i John L. Fowlkes, red. Diabetic Bone Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-16402-1.

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9

Diel, Ingo J., M. Kaufmann i G. Bastert, red. Metastatic Bone Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78596-2.

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10

Roodman, G. David, red. Myeloma Bone Disease. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-554-5.

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11

Randall, R. Lor, red. Metastatic Bone Disease. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-5662-9.

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12

Roodman, G. David. Myeloma bone disease. New York: Humana, 2010.

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13

D, Tiegs Robert, red. Metabolic bone disease. Philadelphia: Saunders, 1989.

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14

D, Tiegs Robert, red. Metabolic bone disease. Philadelphia: Saunders, 1990.

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15

Patel, Vinood B., i Victor R. Preedy, red. Biomarkers in Bone Disease. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7693-7.

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16

Preedy, Victor R., red. Biomarkers in Bone Disease. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7745-3.

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17

J, Maricic Michael, i Gluck Oscar S. 1949-2003, red. Bone disease in rheumatology. Philadelphia: Lippincott Williams & Willkins, 2005.

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18

A, Morris H., Need A. G i Nordin B. E. C, red. Metabolic bone and stone disease. Wyd. 3. Edinburgh: Churchill Livingstone, 1993.

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19

C, Nordin B. E., Need A. G i Morris H. A, red. Metabolic bone and stone disease. Wyd. 3. Edinburgh: Churchill Livingstone, 1993.

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20

McKillop, James H. Benign and malignant bone disease. Edinburgh: Churchill Livingstone, 1990.

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21

Paul, Grech, red. Diagnosis of metabolic bone disease. London: Chapman and Hall Medical, 1985.

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22

I, Tovey F., i Stamp T. C. B, red. The measurement of metabolic bone disease. New York: Parthenon Pub. Group, 1995.

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23

Rachel, Ives, i ScienceDirect (Online service), red. The bioarchaeology of metabolic bone disease. Amsterdam: Elsevier/Academic Press, 2008.

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24

C, Stevenson John, red. New techniques in metabolic bone disease. London: Wright, 1990.

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25

Orthopaedic management of metastatic bone disease. St. Louis: Mosby, 1988.

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26

Parker, James N., i Philip M. Parker. Paget's disease: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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27

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0144.

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Streszczenie:
Paget's disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.
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28

Kanis, J. A. Pathophysiology and Treatment of Paget's Disease of Bone. Taylor & Francis Ltd, 1991.

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29

Paget's Disease of Bone: Comments by Eight Specialists. Excerpta Medica, An Elsevier Company, 1988.

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30

Kanis, John A. Pathophysiology and Treatment of Paget's Disease of Bone. Carolina Academic Press, 1991.

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31

Javaid, Kassim. Paget’s disease of bone. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0274.

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Paget’s disease of bone is an uncommon bone disorder with increased bone resorption and disorganized bone formation of woven bone. Its cause is unclear; there is a clear genetic component but additional environmental factors are important, given the reduction in severity and prevalence in the UK. Paget’s disease is usually asymptomatic and detected by an unexplained raised alkaline phosphatase on routine biochemistry. Symptoms include focal bone pain, including headache. Other symptoms include bone deformity and complications such as fracture and nerve conduction. Paget’s disease can sometimes present with immobilization-associated hypercalcaemia or high-output cardiac failure, and rarely can transform to an osteosarcoma. This chapter addresses the clinical features, diagnosis, and management of Paget’s disease of bone.
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32

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0144_update_001.

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Streszczenie:
Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.
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33

Advances in Pathobiology and Management of Paget's Disease of Bone. Elsevier, 2016. http://dx.doi.org/10.1016/c2015-0-02298-5.

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34

Reddy, Sakamuri V. Advances in Pathobiology and Management of Paget's Disease of Bone. Elsevier Science & Technology Books, 2016.

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35

Singer, F. R. Paget's Disease of Bone: Clinical Assessment, Present and Future Therapy. Elsevier Science Ltd, 1991.

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36

Reddy, Sakamuri V. Advances in Pathobiology and Management of Paget's Disease of Bone. Elsevier Science & Technology Books, 2016.

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37

Singer, Frederick. Paget's Disease of Bone: Clinical Assessment, Present and Future Therapy Proceedings of the Symposium on the Treatment of Paget's Disease of Bone, Held October 20, 1989 in New York City. Springer, 2012.

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38

Paget's Disease of Bone: Clinical Assessment, Present and Future Therapy Proceedings of the Symposium on the Treatment of Paget's Disease of Bone, held October 20, 1989 in New York City. Springer, 2012.

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39

Singer, Frederick. Paget's Disease of Bone: Clinical Assessment, Present and Future Therapy Proceedings of the Symposium on the Treatment of Paget's Disease of Bone, Held October 20, 1989 in New York City. Springer London, Limited, 2012.

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40

Kanis, John A. Pathophysiology and Treatment of Pagets Disease of Bone. Wyd. 2. Informa Healthcare, 1998.

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41

Wordsworth, Paul. Metabolic disease of skeleton and inherited disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.010001.

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♦ Classic metabolic bone diseases include osteoporosis, osteomalacia, Paget’s disease, and parathyroid bone disease♦ Heritable disorders of the skeleton include numerous osteochrondrodysplasias, Marfan syndrome, and Ehlers-Danlos syndrome♦ Investigation of short stature is indicated for those below 0.4 percentile, with skeletal disproportion and/or progressive shortness♦ Genetic mutations for most of these conditions have been identified but clinical/radiographic features are usually diagnostic.
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42

Keen, Richard W. Inflammatory and metabolic bone disorders of the pelvis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.007016.

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43

Understanding Paget's disease. [Bethesda, Md.?]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1985.

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44

Sharpe, Paul T. Molecular Biology of Paget's Disease. Springer London, Limited, 2013.

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45

Carton, James. Osteoarticular pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0017.

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This chapter discusses osteoarticular pathology, including osteoporosis, osteopetrosis, rickets and osteomalacia, Paget’s disease, osteomyelitis, osteoarthritis, rheumatoid arthritis, spondyloarthropathies, crystal arthropathies, septic arthritis, periprosthetic reactions, soft tissue and bone tumours, benign soft tissue tumours, malignant soft tissue tumours, benign bone tumours, and malignant bone tumours.
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46

Sharpe, Paul. The Molecular Biology of Paget's Disease. Springer, 2014.

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47

T, Sharpe Paul, red. The molecular biology of Paget's disease. New York: Springer, 1996.

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48

CHEVY, Chet. Paget's Disease of the Breast Treatment Handbook: Paget's Disease of the Breast Explained from ILL to HEALTH. Independently Published, 2022.

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49

Gikas, Panagiotis D., i Timothy W. R. Briggs. Metastatic bone disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.002007.

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♦ Metastatic pathological fractures rarely unite, even if stabilized♦ Never rush to fix a pathological fracture; traction or splintage will suffice while investigations are performed and surgical intervention discussed♦ When surgery is indicated for spinal metastases, both decompression and stabilization are generally required♦ Implants should allow immediate weight-bearing and last the lifetime of the patient♦ Always use a multidisciplinary team.
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50

Metabolic bone disease. Philadelphia: Saunders, 1991.

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